Pulmonary edema remains a major clinical problem and future advances in therapy require a broad view of the many factors which influence the development and recovery from edema. I propose that normal alveolo-capillary permeability depends upon normal cellular energy metabolism and possibly upon an ability to increase production of high energy phosphate bonds. I plan to test this hypothesis by studying edema formation and resolution in the isolated perfused rat lung. Inhibitors of metabolism and potential mediators of vascular permeability will be used to study the relationship between normal metabolism and permeability.